DACH1, a novel target of miR-218, participates in the regulation of cell viability, apoptosis, inflammatory response, and epithelial-mesenchymal transition process in renal tubule cells treated by high-glucose

High glucose-mediated tubular injury contributes to the development and progression of diabetic nephropathy through renal tubulointerstitial fibrosis. V-set immunoglobulin-domain-containing 4 (VSIG4), a B7 family-related protein, is a complement receptor. Although the role of epithelial–mesenchymal transition (EMT) has been reported in several diseases, little is known about its relationship with VSIG4 under diabetic conditions. This study aimed to investigate the role of VSIG4 in human tubule cells stimulated by high glucose (HG, 55 mM). HG upregulated both mRNA and protein levels of VSIG4 in proximal tubule cells (HK-2 cells) and Madin Darby Canine Kidney cells. These upregulations were accompanied by increased expression of mesenchymal markers such as fibronectin, N-cadherin, matrix metalloproteinase 9, and vimentin, and by decreased expression of the epithelial marker, E-cadherin. The siRNA-mediated inhibition of VSIG4 in HK-2 cells restored the dysregulation of EMT in cells. Interestingly, VSIG4 inhibition did not affect the expression of transforming growth factor (TGF)-β, whereas inhibition of TGF-β reduced VSIG4 expression, subsequently suppressing fibrosis markers. These findings suggest that VSIG4 plays an important role in mediating renal tubular EMT through the downstream action of HG-induced TGF-β activation.

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Silenced SNHG1 Inhibited Epithelial-Mesenchymal Transition and Inflammatory Response of ARPE-19 Cells Induced by High Glucose

Journal of Inflammation Research ◽

10.2147/jir.s299010 ◽

2021 ◽

Vol Volume 14 ◽

pp. 1563-1573

Author(s):

Jing Yang ◽

Kun Yang ◽

Xuxia Meng ◽

Penghui Liu ◽

Yudong Fu ◽

...

Keyword(s):

Inflammatory Response ◽

High Glucose ◽

Epithelial Mesenchymal Transition ◽

Mesenchymal Transition

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MicroRNA-144 Suppresses Prostate Cancer Growth and Metastasis by Targeting EZH2

Technology in Cancer Research & Treatment ◽

10.1177/1533033821989817 ◽

2021 ◽

Vol 20 ◽

pp. 153303382198981

Author(s):

Xin-bo Sun ◽

Yong-wei Chen ◽

Qi-sheng Yao ◽

Xu-hua Chen ◽

Min He ◽

...

Keyword(s):

Prostate Cancer ◽

Cell Viability ◽

Cell Apoptosis ◽

Epithelial Mesenchymal Transition ◽

Luciferase Reporter ◽

Mesenchymal Transition ◽

Proliferation And Apoptosis ◽

High Incidence ◽

Inhibit Cell Proliferation

Background: Prostate cancer is a common malignant tumor with a high incidence. MicroRNAs (miRNAs) have been shown to be important post-transcriptional regulators during tumorigenesis. This study aimed to explore the effect of miR-144 on PCa proliferation and apoptosis. Material and Methods: The expression of miR-144 and EZH2 were examined in clinical PCa tissues. PCa cell line LNCAP and DU-145 was employed and transfected with miR-144 mimics or inhibitors. The correlation between miR-144 and EZH2 was verified by luciferase reporter assay. Cell viability, apoptosis and migratory capacity were detected by CCK-8, flow cytometry assay and wound healing assay. The protein level of EZH2, E-Cadherin, N-Cadherin and vimentin were analyzed by western blotting. Results: miR-144 was found to be negatively correlated to the expression of EZH2 in PCa tissues. Further studies identified EZH2 as a direct target of miR-144. Moreover, overexpression of miR-144 downregulated expression of EZH2, reduced cell viability and promoted cell apoptosis, while knockdown of miR-144 led to an inverse result. miR-144 also suppressed epithelial-mesenchymal transition level of PCa cells. Conclusion: Our study indicated that miR-144 negatively regulate the expression of EZH2 in clinical specimens and in vitro. miR-144 can inhibit cell proliferation and induce cell apoptosis in PCa cells. Therefore, miR-144 has the potential to be used as a biomarker for predicting the progression of PCa.

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LOX-1 and cancer: an indissoluble liaison

Cancer Gene Therapy ◽

10.1038/s41417-020-00279-0 ◽

2021 ◽

Author(s):

M. Murdocca ◽

C. De Masi ◽

S. Pucci ◽

R. Mango ◽

G. Novelli ◽

...

Keyword(s):

Tumor Progression ◽

Epithelial Mesenchymal Transition ◽

Vascular Endothelial Cells ◽

Transition Process ◽

Receptor Protein ◽

Pancreatic Tumors ◽

Tumor Evolution ◽

Mesenchymal Transition ◽

Angiogenic Proteins

AbstractRecently, a strong correlation between metabolic disorders, tumor onset, and progression has been demonstrated, directing new therapeutic strategies on metabolic targets. OLR1 gene encodes the LOX-1 receptor protein, responsible for the recognition, binding, and internalization of ox-LDL. In the past, several studied, aimed to clarify the role of LOX-1 receptor in atherosclerosis, shed light on its role in the stimulation of the expression of adhesion molecules, pro-inflammatory signaling pathways, and pro-angiogenic proteins, including NF-kB and VEGF, in vascular endothelial cells and macrophages. In recent years, LOX-1 upregulation in different tumors evidenced its involvement in cancer onset, progression and metastasis. In this review, we outline the role of LOX-1 in tumor spreading and metastasis, evidencing its function in VEGF induction, HIF-1alpha activation, and MMP-9/MMP-2 expression, pushing up the neoangiogenic and the epithelial–mesenchymal transition process in glioblastoma, osteosarcoma prostate, colon, breast, lung, and pancreatic tumors. Moreover, our studies contributed to evidence its role in interacting with WNT/APC/β-catenin axis, highlighting new pathways in sporadic colon cancer onset. The application of volatilome analysis in high expressing LOX-1 tumor-bearing mice correlates with the tumor evolution, suggesting a closed link between LOX-1 upregulation and metabolic changes in individual volatile compounds and thus providing a viable method for a simple, non-invasive alternative monitoring of tumor progression. These findings underline the role of LOX-1 as regulator of tumor progression, migration, invasion, metastasis formation, and tumor-related neo-angiogenesis, proposing this receptor as a promising therapeutic target and thus enhancing current antineoplastic strategies.

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High glucose-induced epithelial-mesenchymal transition contributes to the upregulation of fibrogenic factors in retinal pigment epithelial cells

International Journal of Molecular Medicine ◽

10.3892/ijmm.2016.2768 ◽

2016 ◽

Vol 38 (6) ◽

pp. 1815-1822 ◽

Cited By ~ 9

Author(s):

Di Che ◽

Ti Zhou ◽

Yuqing Lan ◽

Jinye Xie ◽

Haijun Gong ◽

...

Keyword(s):

Epithelial Cells ◽

High Glucose ◽

Retinal Pigment Epithelial ◽

Epithelial Mesenchymal Transition ◽

Retinal Pigment ◽

Retinal Pigment Epithelial Cells ◽

Mesenchymal Transition ◽

Pigment Epithelial ◽

Pigment Epithelial Cells

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Resveratrol prevents high glucose-induced epithelial–mesenchymal transition in renal tubular epithelial cells by inhibiting NADPH oxidase/ROS/ERK pathway

Molecular and Cellular Endocrinology ◽

10.1016/j.mce.2014.12.010 ◽

2015 ◽

Vol 402 ◽

pp. 13-20 ◽

Cited By ~ 43

Author(s):

Ting He ◽

Xu Guan ◽

Song Wang ◽

Tangli Xiao ◽

Ke Yang ◽

...

Keyword(s):

Epithelial Cells ◽

Nadph Oxidase ◽

High Glucose ◽

Epithelial Mesenchymal Transition ◽

Erk Pathway ◽

Tubular Epithelial Cells ◽

Renal Tubular Epithelial Cells ◽

Mesenchymal Transition ◽

Renal Tubular

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Src-1 and SP2 promote the proliferation and epithelial–mesenchymal transition of nasopharyngeal carcinoma

Open Medicine ◽

10.1515/med-2021-0248 ◽

2021 ◽

Vol 16 (1) ◽

pp. 1061-1069

Author(s):

Jingjing Zhang ◽

Yuanyuan Yang ◽

Hongyu Liu ◽

Hongyi Hu

Keyword(s):

Nasopharyngeal Carcinoma ◽

Cell Viability ◽

Colony Formation ◽

Epithelial Mesenchymal Transition ◽

Southern China ◽

Mrna Level ◽

Migration And Invasion ◽

High Morbidity ◽

Mesenchymal Transition ◽

Steroid Receptor Coactivator

Abstract Nasopharyngeal carcinoma (NPC) is characterized by high morbidity and morality, especially in Southern China. Transcription factors intensively participate in the initiation and development of NPC. This study aimed to investigate the roles of Src-1 in NPC. mRNA level was determined by qRT-PCR. Western blot was carried out for the protein level. CCK-8 assay was performed to determine cell viability, colony formation for NPC cell proliferation, and transwell for cell migration and invasion ability. The results showed Steroid receptor coactivator 1 (Src-1) was overexpressed in SNE-2 and 6-10B. The expression of Src-1 and SP2 was in positive correlation. Overexpression of Src-1 promoted the cell viability, colony formation, and epithelial–mesenchymal transition (EMT), manifested by the increase of migration and invasion ability, while knockdown of Src-1 exerted opposite effects. Additionally, knockdown or overexpression of SP2 reversed the effects of overexpressed or downregulated Src-1, which was reversed by the depletion of SP2. Moreover, Src-1 interacted with SP2 to regulate EMT-related genes such as E-cad, N-cad, Vimentin, and ZEB1, and proliferation- and apoptosis-related genes, such as bax, cytochrome c, and cleaved caspase3 and bcl-2. Thus, blocking the interaction between Src-1 and SP2 may be a therapeutic target for inhibiting the metastasis of NPC.

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